Orphan nuclear hormone receptor NR4A1 interacts with HPV16 E2 regulatory protein

Olejnik-Schmidt, Agnieszka; Schmidt, Marcin; Goździcka-Józefiak, Anna

doi:10.2478/s11658-006-0010-x

Cited by 5 publications

(3 citation statements)

References 23 publications

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“…We speculate that binding of SMN1 to E2 might thus favor apoptosis. A yeast-two hybrid screen also identified NR4A1 as an interacting partner of HPV16 E2 [70]. This protein is a member of the nuclear-receptor superfamily and plays a role in regulating cell growth and apoptosis [71].…”

Section: The E2 Interactomementioning

confidence: 99%

The HPV E2-Host Protein-Protein Interactions: A Complex Hijacking of the Cellular Network

Muller

Demeret

2012

TOVJ

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Over 100 genotypes of human papillomaviruses (HPVs) have been identified as being responsible for unapparent infections or for lesions ranging from benign skin or genital warts to cancer. The pathogenesis of HPV results from complex relationships between viral and host factors, driven in particular by the interplay between the host proteome and the early viral proteins. The E2 protein regulates the transcription, the replication as well as the mitotic segregation of the viral genome through the recruitment of host cell factors to the HPV regulatory region. It is thereby a pivotal factor for the productive viral life cycle and for viral persistence, a major risk factor for cancer development. In addition, the E2 proteins have been shown to engage numerous interactions through which they play important roles in modulating the host cell. Such E2 activities are probably contributing to create cell conditions appropriate for the successive stages of the viral life cycle, and some of these activities have been demonstrated only for the oncogenic high-risk HPV. The recent mapping of E2-host protein-protein interactions with 12 genotypes representative of HPV diversity has shed some light on the large complexity of the host cell hijacking and on its diversity according to viral genotypes. This article reviews the functions of E2 as they emerge from the E2/host proteome interplay, taking into account the large-scale comparative interactomic study.

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Section: The E2 Interactomementioning

confidence: 99%

The HPV E2-Host Protein-Protein Interactions: A Complex Hijacking of the Cellular Network

Muller

Demeret

2012

TOVJ

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“…Adult male Wistar rats were randomly divided into four groups (three different degree loading stress groups and one control group) as described (Olejnik-Schmidt et al 2006). The stress group animals were placed separately into an adjustable restraint cage for 6 h per day (from 9:00 A.M. to 15:00 P.M.) for varying periods of time: 1, 2 and 3 weeks.…”

Section: Rat Model Of Chronic Restraint Stressmentioning

confidence: 99%

NGFI-B targets mitochondria and induces cardiomyocyte apoptosis in restraint-stressed rats by mediating energy metabolism disorder

Wang¹,

Liu²,

Kong³

et al. 2009

Cell Stress and Chaperones

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NGFI-B/Nur77/TR3, originally identified as an immediate-early gene rapidly induced by serum and growth factors, is a member of the steroid hormone nuclear receptor superfamily with no identified endogenous ligand. NGFI-B induces apoptosis in a number of cell lineages exposed to proapoptotic stimuli by directly targeting the mitochondria, inducing cytochrome c release. The present study was designed to determine the role of NGFI-B in cardiomyocytes of restraintstressed rats. The NGFI-B content was increased in mitochondria and reduced in plasma as apoptosis increased. Analysis showed that NGFI-B induces cardiomyocyte apoptosis in restraint-stressed rats by mediating mitochondrial energy metabolism disorder. Several novel mitochondrial proteins, which correlate with NGFI-B, were reported in cardiomyocyte apoptosis of restraint-stressed rats. Five proteins associated with NGFI-B participate directly in mitochondrial energy metabolism. Studies of mitochondrial respiratory efficiency and ATP synthase activity strongly support the findings. These results provide significant information for comprehensively understanding the cellular mechanism of cardiovascular diseases.

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“…The expression of NR4A1 may be induced via transactivation by several viruses, such as hepatitis B virus, human T-lymphotropic virus type 1 and adenovirus (Chen et al , 1998; Granberg et al , 2006; Lee et al , 2001; Liu et al , 1999). Furthermore, the interaction of Epstein–Barr virus nuclear antigen 2 with NR4A1 retains NR4A1 in the nucleus and is thought to be a viral strategy to block apoptosis, whilst the interaction of NR4A1 with human papillomavirus 16 E2 protein has been proposed to modulate viral genome transcription (Lee et al , 2002, 2004; Olejnik-Schmidt et al , 2006). In the present study, we analysed the expression of NR4A1 during HCV infection and explored its role in the HCV life cycle.…”

Section: Introductionmentioning

confidence: 99%

Nuclear receptor 4 group A member 1 determines hepatitis C virus entry efficiency through the regulation of cellular receptor and apolipoprotein E expression

Zhu

Pei

Jin

et al. 2014

Journal of General Virology

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Orphan nuclear receptor subfamily 4 group A member 1 (NR4A1) is a transcription factor stimulated by many factors and plays pivotal roles in metabolism, proliferation and apoptosis. In this study, the expression of NR4A1 in Huh7.5.1 cells was significantly upregulated by hepatitis C virus (HCV) infection. The silencing of NR4A1 inhibited the entry of HCV and reduced the specific infectivity of secreted HCV particles but had only minor or no effect on the genome replication and translation, virion assembly and virus release steps of the virus life cycle. Further experiments demonstrated that the silencing of NR4A1 affected virus entry through pan-downregulation of the expression of HCV receptors scavenger receptor BI, occludin, claudin-1 and epidermal growth factor receptor but not CD81. The reduced specific infectivity of HCV in the knockdown cells was due to decreased apolipoprotein E (ApoE) expression. These results explain the delayed spread of HCV in NR4A1 knockdown Huh7.5.1 cells. Thus, NR4A1 plays a role in HCV replication through regulating the expression of HCV receptors and ApoE, and facilitates HCV entry and spread.

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Orphan nuclear hormone receptor NR4A1 interacts with HPV16 E2 regulatory protein

Cited by 5 publications

References 23 publications

The HPV E2-Host Protein-Protein Interactions: A Complex Hijacking of the Cellular Network

The HPV E2-Host Protein-Protein Interactions: A Complex Hijacking of the Cellular Network

NGFI-B targets mitochondria and induces cardiomyocyte apoptosis in restraint-stressed rats by mediating energy metabolism disorder

Nuclear receptor 4 group A member 1 determines hepatitis C virus entry efficiency through the regulation of cellular receptor and apolipoprotein E expression

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